Institute of Social and Preventive Medicine (IUMSP), Lausanne University Hospital, Lausanne, Switzerland.
PLoS Med. 2013;10(7):e1001479. doi: 10.1371/journal.pmed.1001479. Epub 2013 Jul 2.
Socioeconomic adversity in early life has been hypothesized to "program" a vulnerable phenotype with exaggerated inflammatory responses, so increasing the risk of developing type 2 diabetes in adulthood. The aim of this study is to test this hypothesis by assessing the extent to which the association between lifecourse socioeconomic status and type 2 diabetes incidence is explained by chronic inflammation.
We use data from the British Whitehall II study, a prospective occupational cohort of adults established in 1985. The inflammatory markers C-reactive protein and interleukin-6 were measured repeatedly and type 2 diabetes incidence (new cases) was monitored over an 18-year follow-up (from 1991-1993 until 2007-2009). Our analytical sample consisted of 6,387 non-diabetic participants (1,818 women), of whom 731 (207 women) developed type 2 diabetes over the follow-up. Cumulative exposure to low socioeconomic status from childhood to middle age was associated with an increased risk of developing type 2 diabetes in adulthood (hazard ratio [HR] = 1.96, 95% confidence interval: 1.48-2.58 for low cumulative lifecourse socioeconomic score and HR = 1.55, 95% confidence interval: 1.26-1.91 for low-low socioeconomic trajectory). 25% of the excess risk associated with cumulative socioeconomic adversity across the lifecourse and 32% of the excess risk associated with low-low socioeconomic trajectory was attributable to chronically elevated inflammation (95% confidence intervals 16%-58%).
In the present study, chronic inflammation explained a substantial part of the association between lifecourse socioeconomic disadvantage and type 2 diabetes. Further studies should be performed to confirm these findings in population-based samples, as the Whitehall II cohort is not representative of the general population, and to examine the extent to which social inequalities attributable to chronic inflammation are reversible.
人们推测，早期生活中的社会经济逆境会“编程”出一种易受影响的表型，使炎症反应过度，从而增加成年后患 2 型糖尿病的风险。本研究旨在通过评估生命历程社会经济地位与 2 型糖尿病发病之间的关联在多大程度上可以用慢性炎症来解释，来验证这一假设。
我们使用来自英国白厅 II 研究的数据，这是一项 1985 年建立的前瞻性职业队列研究。反复测量了 C 反应蛋白和白细胞介素-6 等炎症标志物，18 年的随访（1991-1993 年至 2007-2009 年）监测 2 型糖尿病的发病情况（新发病例）。我们的分析样本包括 6387 名非糖尿病参与者（1818 名女性），其中 731 名（207 名女性）在随访期间患上 2 型糖尿病。从儿童到中年累积接触低社会经济地位与成年后患 2 型糖尿病的风险增加相关（低累积生命历程社会经济评分的危险比[HR] = 1.96，95%置信区间：1.48-2.58，低-低社会经济轨迹的 HR = 1.55，95%置信区间：1.26-1.91）。生命历程中社会经济逆境累积与 2 型糖尿病相关的超额风险的 25%和低-低社会经济轨迹与 2 型糖尿病相关的超额风险的 32%归因于慢性炎症升高（95%置信区间为 16%-58%）。
在本研究中，慢性炎症解释了生命历程中社会经济劣势与 2 型糖尿病之间关联的很大一部分。应在基于人群的样本中进一步开展研究以验证这些发现，并研究归因于慢性炎症的社会不平等在多大程度上是可以逆转的。
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